Cases reported "Disease Progression"

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1/10. Does amniotomy influence the prognosis of babies in cases with severe chorioamnionitis? Report of a twin pregnancy with varying outcome.

    We report our experience in a woman with a twin pregnancy. The patient suffered severe escherichia coli chorioamnionitis and the outcomes were different between the two babies after birth. The first baby had only a mild infection, but the second suffered sepsis and subsequent perinatal death. These differences in outcome appeared to be due to amniotomy performed for the first baby after late labor stage I to augment uterus contractions. Removal of infectious amniotic fluid from the amniotic cavity might thus have prevented the spread of the chorioamnionitis. E. coli sometimes causes severe infection during pregnancy and the perinatal period. In this case, a large number of enteropathogenic E. coli (serotype O-6) was cultured from blood, stool, pharyngeal swab, gastric juice and puncture fluid from the thoracic cavity of the second baby. O-6 is classified an enterotoxigenic strain mainly causing diarrhea because of endotoxin released from bacteria. O-6 has not hitherto been reported as a cause of severe infection in chorioamnionitis and perinatal sepsis.
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2/10. meningeal carcinomatosis manifested as bilateral progressive sensorineural hearing loss.

    OBJECTIVE: meningeal carcinomatosis is defined as the diffuse infiltration of the leptomeninges and subarachnoid space by malignant cells metastasizing from systemic cancer. The authors describe a rare case of meningeal carcinomatosis initially appearing as bilateral progressive sensorineural hearing loss. PATIENT: A 57-year-old man with lung cancer was referred to the authors' clinic because of progressive hearing loss, tinnitus, dizziness, and blurred vision for 1 month. RESULTS: magnetic resonance imaging revealed abnormal leptomeningeal enhancement. meningeal carcinomatosis was diagnosed by the detection of malignant cells in the cerebrospinal fluid after lumbar puncture. The patient died 1 year after diagnosis. CONCLUSIONS: meningeal carcinomatosis must be considered in the differential diagnosis in cancer patients with bilateral progressive sensorineural hearing loss. gadolinium-enhanced magnetic resonance imaging is a useful complementary diagnostic tool before lumbar puncture.
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3/10. brachial plexus neuropathy as unusual onset of diffuse neurolymphomatosis.

    We present a patient with a large B cell gastric lymphoma in total remission who, after 4 months, developed a fatal progressive peripheral neuropathy with an unusual early involvement of the right brachial plexus. No evidence of lymphoma was found at whole body computed tomography, magnetic resonance imaging of the head, cervical spine and right brachial plexus, bone marrow biopsy or repeated lumbar punctures. The diagnosis of neurolymphomatosis was made only at postmortem examination.
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4/10. diplopia in a patient with carcinomatous meningitis: a case report and review of the literature.

    In a patient with a history of malignancy, an isolated neurologic sign or symptom may indicate metastasis to the central nervous system. To exclude this possibility, a lumbar puncture should still be performed after a nondiagnostic cranial computed tomography (CT) scan even in the absence of signs of infection. A case is presented of a 59 year-old man recently diagnosed with non-Hodgkin's lymphoma that presented to the Emergency Department (ED) with the sole complaint of diplopia. Examination was unremarkable except for a left abducens nerve palsy. Cranial CT scan was normal but initial cerebrospinal fluid results were suggestive of carcinomatous meningitis, and cytology results later confirmed this diagnosis. A review of diplopia and carcinomatous meningitis is presented, along with a suggested conservative diagnostic algorithm for cancer patients presenting with neurologic signs or symptoms.
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5/10. Progression of a posterior communicating artery infundibulum into an aneurysm in a patient with alagille syndrome. Case report.

    The authors present a case in which a posterior communicating artery (PCoA) infundibulum progressed into an aneurysm in a patient with alagille syndrome (arteriohepatic dysplasia). The 3-mm PCoA infundibulum had been noted on angiography studies obtained 5 years earlier, prior to clip occlusion of a basilar tip aneurysm. Recently, the patient presented to the emergency department with the sudden onset of headache and decreased mental status. A computerized tomography scan of the head with three-dimensional angiography revealed no gross subarachnoid hemorrhage, but did demonstrate a 5-mm PCoA aneurysm. Lumbar puncture demonstrated xanthochromia and a large quantity of red blood cells. The patient underwent open surgery for aneurysm clip occlusion and obtained a good recovery. This case illustrates the small but growing number of examples of infundibulum progression. It also indicates the need for a close follow up in patients with congenital abnormalities that may pose an increased risk for what has traditionally been considered a benign lesion.
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6/10. Congenital trypanosomiasis.

    The last successfully treated case of congenital trypanosomiasis in zambia was in October 1978, with detailed analysis of immunoglobulins, illustrating the waning of blood and serum levels of IgA, IgG, and IgM during treatment, up to 99 days after treatment. Twenty-five years later, we report on a case of congenital trypanosomiasis. The disease is now rare and can be missed or dismissed as retroviral disease, particularly in adults. The main unusual symptoms were the prolonged intermittent convulsions in an otherwise well infant. Management of the disease is now more interdisciplinary, resources for laboratory support are fewer, lumbar puncture is more relevant, and antitrypanosomal drugs are more difficult to obtain. The mother died within one week of hospitalization and the infant initially responded to three doses of suramin and 3 weeks of melsopropol. Convulsions ceased during the second round of melsopropol. Unfortunately, the infant died of nosocomial infection.
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7/10. Rapidly progressive spinal muscular atrophy in an ambulatory 2-year-old male.

    A 2-year 9-month-old male was referred for gait disturbances. Main complaints were abnormal gait with frequent falls observed as soon as he began to walk unaided, at 18 months of age. The first neurologic examination revealed symmetric and proximal weakness in the lower limbs with difficulty running and walking upstairs. Deep tendon reflexes were decreased, and generalized hypotonia was observed. Three months later, at 3 years of age, he had lost independent gait, and 1 month later he could not stand unaided. dna analysis revealed homozygous deletion in exons 7 and 8 of SMN1 gene, confirming the diagnosis of spinal muscular atrophy. According to the current classification, this patient would be classified as spinal muscular atrophy type III. The distinctive feature of this case was the short time elapsed (18 months) between onset of spinal muscular atrophy and the age at which he lost ambulation. This patient reinforces the notion that late onset of symptoms in spinal muscular atrophy and acquisition of independent gait do not exclude a rapidly progressive motor deterioration, which is important when talking with families about outcome. In those rapidly progressive cases, when promptly available, testing for SMN1 gene will prevent unnecessary, invasive, or uncomfortable procedures such as lumbar puncture, electromyography, or spinal cord magnetic resonance imaging.
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8/10. Bilateral visual loss complicating liposuction in a patient with idiopathic intracranial hypertension.

    A 34-year-old obese woman developed blurred vision in both eyes soon after large-volume liposuction of the dorsum and gluteus region bilaterally associated with abdominal dermolipectomy. An ophthalmic examination revealed severe bilateral visual loss and pallid optic disc edema. The patient gave a history of transient obscurations of vision in the past. neuroimaging studies were non-revealing, but a lumbar puncture disclosed a markedly elevated intracranial pressure. The patient was diagnosed as having had bilateral ischemic optic neuropathy superimposed on pre-existing idiopathic intracranial hypertension (IIH). acetazolamide treatment was used. Some visual improvement occurred, and optic disc edema evolved into severe optic disc pallor. This case shows that visual loss from optic disc infarction may be a devastating complication of high-volume liposuction in patients with underlying IIH. Because liposuction is frequently performed on obese patients, physicians should screen for signs and symptoms of IIH before undertaking this procedure.
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9/10. Progressive visual loss and motility deficit.

    A 63-year-old female with known stage III, low grade non-Hodgkin's lymphoma presented with progressive visual loss in the left eye and binocular diplopia in all positions of gaze. The left globe was almost immotile. Two MRI's of the orbit were interpreted as normal. Lumbar puncture did not reveal abnormal cytology. Although orbital apex involvement is uncommon in non-Hodgkin's lymphoma, the patient's clinical findings clearly indicated a lesion in this area, which was confirmed by a third MRI. review of one of the initial films showed evidence of orbital apex involvement. To prevent diagnostic delay and unnecessary repeat imaging, the clinical diagnosis of orbital apex syndrome should be clearly communicated to the radiologist. Prompt recognition of orbital apex syndrome may improve visual outcome.
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10/10. cerebrospinal fluid investigations for neurometabolic disorders.

    Careful clinical delineation and advances in analytical methods have opened new possibilities for the detection of inherited neurometabolic disorders, some of which require specific CSF analyses for diagnosis. Although patients suffering from these disorders have recognizable phenotypes, there are strong indications that remain many undiagnosed, leading to a continuation of futile diagnostic searches and, for most disorders, withholding of available rational therapy. As there is still widespread uncertainty about when to perform specialist CSF investigations, it is the aim of this paper to define the place for CSF investigations in the diagnostic work-up of a child with an encephalopathy of unknown origin. Most neurometabolic disorders can be identified through serum, plasma and urine analyses in conjunction with neuroradiological investigations. Whenever CSF investigations are performed, the analysis should include quantitative determination of lactate, pyruvate and amino acids, the latter by methods especially suited for CSF, in addition to cells, glucose, protein, immunoglobulin classes, specific immunoglobulins, and an evaluation of the blood-brain barrier. If the disease course is non-progressive or if extracerebral symptoms are present in addition to an encephalopathy, e.g. endocrinological, hepatic, muscular or renal symptoms, investigations of metabolites in CSF over and above lactate, pyruvate and amino acids are generally noncontributary. Specific CSF investigations, which are discussed in detail, test metabolic pathways of brain metabolism, especially of neurotransmission. For a successful diagnosis of these defects, analyses must be planned individually, before CSF samples are taken, based on family history, clinical findings and disease course. Different determinations require different logistics from taking of the sample to shipment. One indication for specialized CSF analyses including biogenic monoamines and GABA is severe neonatal/infantile epileptic encephalopathy. In addition to a therapeutic trial of B6, folinic acid should be tried empirically for two to three days as the emerging syndrome of folinic acid responsive seizures appears to be the underlying cause in a sizable proportion of patients. In later infancy and childhood, defects in the metabolism of the biogenic monoamines may be suspected in patients with (fluctuating) extrapyramidal disorders, in particular Parkinsonism dystonia or more general "athetoid cerebral palsy", and vegetative disturbances. A severe epileptic encephalopathy and progressive mental retardation may be present. neuroimaging findings do not show specific lesions. Determinations of folates and organic acids in CSF appear at present only warrantable individually in special constellations, e.g. classical clinical findings and disease course suggestive of glutaryl-coa dehydrogenase deficiency with repeated negative quantitative analyses of organic acids in urine. The diagnosis of disorders, which require specific analyses of CSF, can only be achieved by conscious diagnostic decisions based on a concept of the respective disease and repeated scrupolous expert clinical evaluation aided by an array of investigations in blood and urine as well as neuroimaging findings. No single one investigation in CSF can serve as a "selective screening" test. A growing awareness of these disorders is needed and should lead to increased and earlier diagnosis of patients through fewer rather than more lumbar punctures.
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